Atkinson M A, Ellis T M
Department of Pathology, College of Medicine, University of Florida, Gainesville, Florida 32610, USA.
J Am Coll Nutr. 1997 Aug;16(4):334-40. doi: 10.1080/07315724.1997.10718694.
Insulin-Dependent Diabetes (IDD) results from an autoimmune destruction of the insulin secreting pancreatic beta cells. The immunological mechanisms underlying the development of IDD as well as the role of environmental agents (e.g., diet, viruses, stress) in the pathogenesis of the disease are the subject of considerable research efforts. Significant attention has recently been directed to a hypothesis that consumption of cows' milk in infancy may trigger the autoimmune process underlying IDD. Early evidence supporting this "cows' milk hypothesis" included case-control studies surveying infant nutrition practices (i.e., breast feeding versus consumption of infant formula) and the subsequent development of IDD. However, intense media interest surrounding a report indicating anti-bovine serum albumin (BSA) immunity as the cause of IDD has lead to heightened public awareness of the issue, and, together with the epidemiological data, prompted The American Academy of Pediatrics to modify its guidelines for infant feeding practices. However, less public and scientific attention has been given toward the observations that many of these case-control studies were retrospective in design and subject to recall bias, narrow in scope in terms of collecting dietary information, and that similar results have not been duplicated in other more recent (and better designed) investigations. Furthermore, the immunological report implicating anti-BSA immunity with the disease has become controversial due to difficulties in conforming the findings, and experiments in animal models closely resembling human IDD have not uniformly supported a role for anti-BSA immunity in the pathogenesis of IDD. Given the significant morbidity and mortality associated with IDD, an improved understanding of the cause of this disorder as well as identifying possible methods for its prevention are essential. However, without additional supporting information, modification of the cows' milk/BSA composition of diets in order to avoid the disease may be premature. Further studies are needed to clearly establish a role for diet in the pathogenesis of IDD.
胰岛素依赖型糖尿病（IDD）是由分泌胰岛素的胰腺β细胞发生自身免疫性破坏所致。IDD发生发展的免疫机制以及环境因素（如饮食、病毒、压力）在该疾病发病机制中的作用是大量研究工作的主题。最近，人们对一个假说给予了极大关注，即婴儿期饮用牛奶可能引发IDD潜在的自身免疫过程。支持这一“牛奶假说”的早期证据包括病例对照研究，这些研究调查了婴儿的营养习惯（即母乳喂养与食用婴儿配方奶粉）以及随后IDD的发生情况。然而，围绕一份表明抗牛血清白蛋白（BSA）免疫是IDD病因的报告，媒体的浓厚兴趣提高了公众对该问题的认识，并且与流行病学数据一起促使美国儿科学会修改了婴儿喂养实践指南。然而，对于许多这些病例对照研究在设计上是回顾性的且存在回忆偏倚、在收集饮食信息方面范围狭窄，以及在其他更新的（且设计更好的）调查中未重复得到类似结果等观察结果，公众和科学界的关注较少。此外，由于难以证实这些发现，将抗BSA免疫与该疾病联系起来的免疫学报告已引发争议，并且在与人类IDD非常相似的动物模型实验中，并非都支持抗BSA免疫在IDD发病机制中的作用。鉴于IDD相关的高发病率和死亡率，更好地理解这种疾病的病因以及确定可能的预防方法至关重要。然而，在没有额外支持信息的情况下，为避免该疾病而改变饮食中的牛奶/BSA成分可能为时过早。需要进一步研究以明确确定饮食在IDD发病机制中的作用。
